Heart support to prevent ventricular remodeling

ABSTRACT

This is a support device that prevents, reduces, and delays remodeling of diseased cardiac tissue, and also decreases the impact of such remodeling on collateral tissue is disclosed. The invention further reinforces abnormal tissue regions to prevent over-expansion of the tissue due to increased afterload and excessive wall tension. As a result, the support device prevents phenomenon such as systolic stretch from occurring and propagating. The support structure maintains and restores diastolic compliance, wall motion, and ejection fraction to preserve heart functionality. As such, the support device prevents and treats cardiomyopathy and congestive heart failure.

CROSS REFERENCE TO RELATED APPLICATION

This application claims priority to provisional U.S. patent applicationSer. No. 60/231,075, filed Sep. 8, 2000, the entirety of which is herebyincorporated by reference.

FIELD OF THE INVENTION

This invention is directed towards the transfer of energy from viabletissue regions to less viable or non-viable regions, thereby preventing,compensating for, or treating tissue responses to ischemia, infarction,or other abnormalities. In particular, this invention is directedtowards the prevention, reduction, and delay of the remodeling ofdiseased cardiac tissue and the prevention and treatment ofcardiomyopathy and congestive heart failure.

BACKGROUND OF THE INVENTION

Ischemic injury causes tissue remodeling over time. This producesdyssynchronous, hypokinetic, dyskinetic or akinetic tissue function. Onemechanism that perpetuates tissue remodeling (termed systolic stretch)occurs when viable ventricular tissue contracts, producing pressure thatcauses less viable or non-viable tissue to be forced outward. Thisbulging of the less viable or non-viable tissue dissipates the pumpingforce of the heart and adversely impacts cardiac output. The heartattempts to compensate for this decrease in cardiac output by increasingcontractility and/or heart rate. However, the degree of systolic stretchprogressively increases over time, continuing to reduce cardiac output,enlarge the volume of remodeled tissue, and exacerbate the potential forrupture of the affected tissue.

One condition that can result from such remodeling is cardiomyopathy, atypically chronic disorder of heart muscle that may involve hypertrophyand obstructive damage to the heart. A current approach for treatingend-stage cardiomyopathy involves resecting a significant portion of theleft ventricular free wall to reduce the size of the left ventricularcavity. The procedure, developed by Randas J. V. Batista, attempts toimprove the relationship between volume, mass, and diameter. In reducingthe volume of the left ventricle, investigators have observed a decreasein mitral regurgitation but a concomitant decrease in diastoliccompliance. This decreases diastolic filling, which adversely impactsthe complete cardiac cycle.

Other approaches for treating cardiomyopathy include reshaping the heartchambers using tethers, balloons, external bands, or other tensionstructures to reduce the end-diastolic diameters of the ventricles. PCTPamphlets WO 98/29041 entitled “Heart Wall Tension Reduction Apparatusand Method”; WO 99/30647 entitled “Valve to Myocardium Tension MembersDevice and Method”; WO 00/06026 entitled “Heart Wall Tension ReductionApparatus and Method”; WO 00/06027 entitled “Stress Reduction Apparatusand Method”; WO 00/06028 entitled “Transventricular Implant Tools andDevices”; WO 00/16700 entitled “External Stress Reduction Device andMethod” describe tethers or bands that change the geometry of the heartand restrict the maximum outer diameters of the ventricles. The tethersare positioned inside the heart and extend from one side of theventricle to the other to exert tension on opposite sides of the heart.The bands are positioned around the epicardial surface of the ventriclesand restrict expansion of the ventricles. The tethers and bands onlylimit local wall tension and maximal end-diastolic diameter; they do notdirectly assist in systolic ejection or diastolic filling of the heart.Nor do they distribute loading over a large region of heart tissue.

SUMMARY OF THE INVENTION

The present invention addresses deficiencies associated with priorapproaches of purely reducing the end-diastolic diameter of the heart orpreventing over-stressing of cardiac tissue. The approach described bythis invention uses a heart support structure to transfer energy, in theform of contraction and expansion, from viable heart tissue to lessviable or non-viable heart tissue. This structure prevents, compensatesfor, or treats tissue responses to ischemia, infarction, or otherabnormalities.

The embodiments of the invention maintain diastolic compliance of thecardiac tissue and synchronize the expansion and contraction of thediseased tissue to that of viable tissue in order to restore systolicejection and diastolic filling. This improves wall motion and betterrestores normal functionality of the heart. As a result, the embodimentsof the invention prevent, reduce, and/or delay remodeling of thediseased tissue, decrease the impact of such remodeling on collateraltissue, and preserve all phases of the cardiac cycle.

The embodiments of the invention are also useful in reinforcing abnormaltissue regions to prevent over-expansion of the tissue due to increasedafterload and excessive wall tension. As a result, the dyssynchrony,hypokinesis, dyskinesis or akinesis, which occurs when tissue remodelsover time, is inhibited. As such, the embodiments of the inventionprevent progressive cardiomyopathy and congestive heart failure.

This invention provides electromagnetic assist devices that takeadvantage of the characteristics of the heart support structure of theinvention to impart contraction and expansion throughout the heart, oralong a specific region of the ventricles. The electromagnetic assistdevice strategically induces magnetic fields throughout individualelectromagnets coupled to the support structure, which causes anattraction or repulsion of the electromagnets and imparts a contractionor expansion of the heart support structure, and transfers such energyto cardiac tissue.

The present invention also provides enhancements to the overall systemto continue to make positioning and securing the heart support structureamenable to less invasive procedures, such an endoscopic, port accessapproaches. In addition, the present invention enables catheterizationapproaches to position and secure the heart support structure.

Further features and advantages of the inventions will be elaborated inthe detailed description and accompanying drawings.

BRIEF DESCRIPTION OF THE DRAWINGS

FIG. 1 is a side view of a heart containing a support structure of thepresent invention attached along an exterior portion of its leftventricle.

FIG. 2 is a side view of a heart containing another support structure ofthe present invention attached along an exterior portion of its leftventricle.

FIG. 3 is a flattened view of a heart support structure of the presentinvention.

FIG. 4 is a flattened view of another heart support structure of thepresent invention.

FIG. 5 is a side view of a heart containing the support structure ofFIG. 4 emanating from the apex of the heart.

FIG. 6 is a side view of a heart containing the support structure ofFIG. 4 emanating from the ischemic or infracted region of the heart.

FIG. 7 is a flattened view of yet another heart support structure of thepresent invention.

FIG. 8 is a side view of a heart containing the support structure ofFIG. 7 emanating from the ischemic or infracted region of the heart.

FIG. 9A is a flattened view of still another heart support structure ofthe present invention in its compressed state.

FIG. 9B is a flattened view of the heart support structure of FIG. 9A inits expanded state.

FIG. 10 is a side view of a heart containing the support structure ofFIG. 9B.

FIG. 11 is a side-sectional view of a heart containing supportstructures of the present invention along the interior surface of theleft ventricle and right ventricle.

FIG. 12A is a perspective view of an anchor used to attach the heartsupport structure of the present invention to tissue.

FIGS. 12B and 12C show top views of two additional anchor embodiments ofthe present invention.

FIG. 12D is a side-sectional view of a heart support structure securedto a tissue surface using the anchor embodiments of FIGS. 12A to 12C.

FIG. 13A is a top view of another anchor embodiment.

FIG. 13B is a side-sectional view of a heart support structure securedto a tissue surface using the anchor embodiment of FIG. 13A.

FIG. 13C is a side-sectional view of a heart support structure securedto a tissue surface using an alternative anchor embodiment.

FIG. 14A is a top view of another anchor embodiment.

FIG. 14B is a side-sectional view of a heart support structure securedto a tissue surface using the anchor embodiment of FIG. 14A.

FIG. 15A is a side view of a heart containing an electromagneticallyinduced assist device that incorporates a heart support structure.

FIG. 15B is an enlarged view of the heart support structure in FIG. 15A.

FIG. 16A is a side view of a heart containing an electromagneticallyinduced assist device that incorporates a heart support structure and issynchronized with the heart's electrical propagation.

FIG. 16B is an enlarged view of the heart support structure in FIG. 16A.

DETAILED DESCRIPTION OF THE INVENTION

The embodiments of the invention are intended to transmit energy fromviable tissue regions to less viable or non-viable regions therebypreventing, compensating for, or treating tissue responses to ischemia,infarction, or other abnormalities. Ischemic injury causes tissueremodeling over time and produces dyssynchronous, hypokinetic,dyskinetic or akinetic tissue function. The embodiments of the inventionprevent, reduce, and/or delay remodeling of diseased cardiac tissue, andalso decrease the impact of such remodeling on collateral tissue. Theembodiments of the invention are also useful in reinforcing abnormaltissue regions to prevent over-expansion of the tissue due to increasedafterload and excessive wall tension. The embodiments of the inventionmaintain and/or restore diastolic compliance, wall motion, and ejectionfraction to preserve heart functionality. As such, the embodiments ofthe invention prevent progression of cardiomyopathy and congestive heartfailure.

The approach described by this invention, which uses a heart supportstructure to transfer energy (in the form of artificial contraction andexpansion) from viable heart tissue to less viable or non-viable hearttissue, addresses the deficiencies of prior approaches, which purelyreduce the end-diastolic diameter of the heart. This invention aids theheart during systolic ejection and diastolic filling to better restorenormal functionality of the heart. The heart support structure controlsthe motion of the heart and synchronizes the contraction and expansionof diseased tissue to that of viable tissue.

The heart support structure also accounts for the natural motion of theheart. As the heart contracts, the cross-sectional diameters of theventricles decrease and the distance from the mitral valve annulus tothe apex of the heart also decreases; as the heart expands, thecross-sectional diameters of the ventricles increase and the distancefrom the mitral valve annulus to the apex of the heart also increases.The optimal ratios of expansion (and contraction) between thecross-sectional diameters of the ventricles and the distance from themitral valve annulus to the apex of the heart may be incorporated in thesupport structure to further preserve heart functionality. The heartsupport structure therefore preserves the wall motion and preventsremodeling of the diseased tissue by inhibiting over-expansion andmaintaining normal actuation of all phases of the cardiac cycle. As aresult, the dyssynchrony, hypokinesis, dyskinesis or akinesis, whichoccurs when tissue remodels over time, is inhibited.

Heart Support Structures

The heart support structure embodiments consist of one or morecomponents designed to exert force against a diseased (e.g., ischemic orinfarcted) region of tissue in response to the contraction or expansionof viable tissue. As such, the support structure transfers energy fromviable tissue to less viable or non-viable tissue to control and forcemovement of injured tissue and prevent remodeling that occurs as aresponse to ischemic injury.

The heart support structures are preferably fabricated from superelastic(pseudoelastic) shape memory alloys, such as nickel titanium.Superelastic materials elastically deform upon exposure to an externalforce and return towards their preformed shape upon reduction or removalof the external force. Superelastic shape memory alloys are capable ofexhibiting stress-induced martensitic behavior; which means theytransform from the preshaped austenitic phase to the softer and moreductile martensite phase upon application of stress and transform backtoward the stronger and harder austenite phase once the stress isremoved. Superelastic shape memory alloys enable straining the materialnumerous times without plastically deforming the material. Superelasticshape memory alloys are also light in weight, biocompatible, and exhibitexcellent tensile strengths such that they may be attached to the heartwithout substantially adding weight or bulk.

The characteristics of superelastic shape memory alloys described abovehighlight their utility in providing a support structure for the heartbecause they withstand continuous and frequent deflections withoutplastically deforming or observing fatigue failures. Superelasticsupport structures may also be elastically deflected into small radii ofcurvature and return towards their preformed configuration once theexternal force causing the deflection is removed. Although other, moreconventional materials such as stainless steel may be used in thisapplication, their geometry is likely to be less fine or compact becausetheir material properties dictate that the total elastic energy storedin a given device is much lower. Other known metal, alloy, andthermoplastic materials plastically deform when deflected into similarradii of curvature, using comparable strains, and are unable to returntowards their original configuration. As such, superelastic supportstructures permit deflections into smaller radii of curvature than othermetals, alloys, and polymers resulting in the ability to withstandlarger strains without failing; they are also capable of exertingsubstantial force when deflected.

We prefer that support structures fabricated from shape memory alloys(e.g., nickel titanium) be engineered to form stress-induced martensite(SIM) at body temperature. The composition of the shape memory alloy ispreferably chosen to produce martensitic transformation temperatures(M_(s) and M_(f)) and austenitic transformation temperatures (A_(s) andA_(f)) such that the alloy exhibits stress induced martensite up to atemperature M_(d), greater than A_(f)

The relative composition of nickel and titanium determines the A_(f) ofthe shape memory allow. For example, nickel titanium having an atomicratio of 51.2% Ni and 48.8% Ti exhibits an A_(f) of approximately −20 C;nickel titanium having an atomic ratio of 50% Ni to 50% Ti exhibits anA_(f) of approximately 100 C (Melzer A, Pelton A. “SuperelasticShape-Memory Technology of Nitinol in Medicine” Min Invas Ther & AlliedTechnol. 2000: 9(2) 59-60).

Preferably the composition and fabrication of the nickel titanium ischosen such that the A_(f) is below 32 C. Such materials are able towithstand strains as high as 10% without plastically deforming. As such,these superelastic materials are capable of elastically exerting forceupon deflection.

Superelastic shape memory alloys that do not exhibit stress-inducedmartensitic behavior at body temperature but enable elastic deformationthrough the range of motion the material is exposed may alternatively beused. Materials other than superelastic shape memory alloys may be usedfor the support structures provided they can be elastically deformedwithin the temperature, stress, and strain parameters required tomaximize the elastic restoring force. Such materials include other shapememory alloys, spring stainless steel 17-7, ELGILOY (Elgiloy LP, Elgin,Ill.), superelastic polymers, etc.

Throughout this description, discussions of external force preferablyrefer to the contraction and/or expansion of viable tissue causing thesupport structure to respond accordingly unless otherwise specified.Alternatively, another external means, artificial, biological, or acombination of artificial and biocompatible means for compressing and/orexpanding the support structure may be used as will be discussed later.

Other materials may be used as a covering to the support structure,including thermoplastics (e.g., polytetrafluoroethylene or PTFE),thermoset plastics (e.g., polyethylene terephthalate, polyester), orsilicone. For example, heart support structures fabricated from nickeltitanium may be covered with expanded PTFE by sintering layers ofexpanded PTFE positioned to encompass the support structure material.Alternatively, the support structures may be coated with silicone, whichwhen allowed to cure produces a covering over the support structure.

The heart support structure may be coated with materials such asparylene or other hydrophilic substrates that are biologically inert andreduce the surface friction. To further reduce the surface friction,metallic or metallic alloy fittings may be electropolished. Evidencesuggests that electropolishing reduces adhesion because of the smoothsurface and low surface tension. Alternatively, the heart supportstructures may be coated with heparin, thromboresistance substances(e.g., glycoprotein IIb/IIIa inhibitors), antiproliferative substances(e.g., Rapamycin), or other coatings designed to prevent adhesion,thrombosis for blood contacting support structures, hyperplasia, orother tissue response that may adversely impact the functionality of theheart support structure. Alternatively, materials such as platinum,gold, tantalum, tin, tin-indium, zirconium, zirconium alloy, zirconiumoxide, zirconium nitrate, phosphatidyl-choline, pyrolytic carbon, orothers may be deposited onto the heart support structure surface usingelectroplating, sputtering vacuum evaporation, ion assisted beamdeposition, vapor deposition, silver doping, boronation techniques, asalt bath, or other coating process.

A still further improvement of the heart support structure that iswithin the scope of the present invention is to include beta or gammaradiation sources on the heart support structure. A beta or gamma sourceisotope having an average half-life of approximately 15 days such asPhosphorous 32 or Palladium 103 may be placed on the heart supportstructure using an ion-implantation process, chemical adhesion process,or other suitable method.

The heart support structure embodiments may be fabricated from a sheetof material cut into the desired pattern and formed (e.g., through aheat treatment process) into the desired geometry (planar, conical,elliptical, cylindrical, or other shape). To produce these heart supportstructures, the raw material may be fabricated into the desired patternby chemical etching, electron discharge machining (EDM), laser cutting,or other manufacturing process. Heart support structures fabricated fromsheet stock are then wrapped or otherwise placed around mandrels havingthe desired resting three-dimensional profile(s) and the heart supportstructure is heated until it assumes this configuration. After heating,the support structure is quenched or otherwise allowed to return to roomtemperature, at which the support structure maintains the preformedshape. If any sides are to be bonded, spot welding, laser welding, orother manufacturing process may be employed.

Alternatively, heart support structure embodiments of the presentinvention may be fabricated from a tube of material having a desiredcross-sectional geometry. The desired pattern of links, anchors, anchorpins, holes, slots, and/or cells may be fabricated on the tubular metalmaterial and may be created using chemical etching, EDM, laser cutting,or other manufacturing process. These heart support structures may bethermally formed into the desired planar or three-dimensional profiledepending on the desired shape of the heart support structure.

FIG. 1 shows a heart containing a support structure 20 secured to theepicardial surface at specific attachment points 22 along a section ofthe left ventricle (LV) 2. A tissue interface 18 may or may not bepositioned between support structure 20 and the epicardium, as will bediscussed below. In this particular embodiment, peripheral links 26extend around the injured tissue 24 (e.g., ischemic or infarcted).Support links 30 extend from peripheral links 26 into the injured tissue24 to provide the structure from which contraction and/or expansionenergy may be transferred from peripheral links 26 to a central region28 of the support structure located throughout the injured tissue 24.The geometry of support structure 20 depends on the location of theinjured tissue. If the injured tissue 24 is on the left ventricular freewall, support structure 20 may be planar or have a slightly curvedthree-dimensional profile. If the injured tissue 24 is apical, supportstructure 20 may be generally conical or approximate one half of anellipsoid.

The support structure embodiment in FIG. 1 is secured to the leftventricle at desired locations throughout a central region 28 within theinjured tissue 24, and along peripheral links 26 and/or support links30. Central region 28 of the support structure may be a discrete pointor a two-dimensional surface, or it may constitute a region of multipleintersecting, interlocking, or adjacent support links 30. Central region28 shown in FIG. 1 consists of four intersecting support links 30; weprefer that a minimum of two intersecting support links 30 be used forthis configuration.

Each support link 30 extends from at least one peripheral link 26located past one end of the injured tissue 24, and attached to viabletissue, to at least one peripheral link 26 located past the opposite endof the injured tissue 24, and attached to viable tissue. An alternativeconfiguration involves individual support links that terminate at thecentral region 28 and are not attached to the other independent supportlinks throughout the central region 28 or using peripheral links.

Peripheral links 26 and support links 30 in the embodiment of FIG. 1 aredesigned for different purposes. Support links 30 are designed to causecorresponding movement of the injured tissue 24 in response tocontraction or expansion of the viable tissue to which support links 30are secured. As such, the support links require sufficient axialstiffness to contract or expand the injured tissue 24 in response tomovement of the proximal ends of the support links located alongperipheral links 26 of support structure 20. Support links 30 must alsohave sufficient flexibility so that they do not hinder movement ofviable tissue between central region 28 and peripheral links 26 of thesupport structure. Peripheral links 26 must be flexible so to be able tomove coincident with contraction and expansion of the left ventricle,and durable enough to maintain the integrity of heart support structure20 despite continued movement of the support structure.

FIG. 2 shows a heart containing another support structure embodiment 20emanating from a central region 28, located within injured tissue 24.The peripheral links 26 for this embodiment do not extend completelyaround the injured tissue, but connect adjacent support links 30 attheir proximal ends and are attached to viable tissue. Support links 30interconnect in central region 28 and the unions are secured to theinjured tissue 24 at attachment points 22. Support links 30 in thisembodiment also interconnect along a middle section 32 located betweencentral region 28 and the periphery of the support structure. Middlesection 32 unions are also secured to the tissue surface at attachmentpoints 22.

It should be noted that middle section 32 may be located along centralregion 28, anywhere between central region 28 and peripheral links 26,and/or along the proximal end of the support structure defined byperipheral links 26. Different middle sections 32 may be positioned atdifferent locations along the tissue surface, depending on the axialstiffness and flexibility requirements of support links 30.

FIGS. 3 and 4 show flattened profiles of two alternative supportstructures of the present invention. Support structures 20 incorporateeight support links 30 that extend from a central point 28 and snaketowards peripheral links 26; a minimum of two support links 30 are usedto form this support structure embodiment. Each turn of a snakingsupport link 30 defines a node 34. The relation of the support links tothe nodes defines the stiffness profile of support structure 20. In FIG.3, support nodes 34 are separated such that the angle A1 betweenadjacent turns of each snaking support link 30 is constant. In FIG. 4,the distance H1 between adjacent support nodes 34 is constant.

The parameters of each support link 30 (width, wall thickness, totallength, and turn length) also influence the stiffness. The stiffnessprofile of the support structure determines the degree of contractionand expansion transferred from viable tissue to injured tissue 24throughout the support structure 20. This profile may be optimizeddepending on the anticipated position of various support links 30relative to anatomic structures and desired responses.

For example, the apex of the heart contracts and expands at a differentdegree than the left ventricular free wall; the right ventricle (RV) ismuch more compliant than the left ventricle. As such, support structure20 must incorporate such profiles to maximize the restoration ofsystolic ejection and diastolic filling. More than one target zone ofinjured tissue may be addressed with a single support structure ormultiple support structures by tailoring the stiffness profile(s) of thesupport structure(s) to ensure the desired contraction and expansionforce is transferred and distributed throughout the surface of thetargeted tissue surface.

FIG. 5 shows the support structure shown in FIG. 4 thermally formed intoa conical geometry and positioned such that central region 28 (in thiscase a point) is located at the apex 14 of the heart. As will bediscusses later, a tissue interface is positioned between supportstructure 20 and the tissue surface. This support structure 20 issecured to the tissue surface at attachment points 22 in central region28, interspersed throughout nodes 34 along support links 30, and alongperipheral links 26. This support structure embodiment is configured totreat apical infarcts or ischemic regions and/or cover both ventricles.As previously discussed, discrete support links 30 may be fabricatedwith various parameters (width, wall thickness, length), node separation(H1), or turn length to impart different stiffness profiles throughoutthe heart.

For example, support links 30 positioned along the right ventricle 4require substantially less stiffness than those positioned along theleft ventricle 2 to impart the same amount of contraction and expansionin the right and left ventricle respectively. In addition, the amount ofcontraction and expansion for the right ventricle differs from that forthe left ventricle, thus the stiffness profile of apically positionedsupport structures must account for the disparity.

FIG. 6 shows the support structure of FIG. 4 emanating from a centralregion 28 positioned within injured tissue 24 located along the leftventricular free wall. Support links 30 extend from a point at centralregion 28 and extend to peripheral links 26 positioned at a desireddistance beyond the injured tissue 24. This particular support structureis configured to isolate the transfer of contraction and expansionenergy from viable tissue, residing outside a border zone of injuredtissue 24, to injured tissue 24.

FIG. 7 shows an alternative support structure embodiment thatinterconnects support links 30 around a circle or other shape used todefine central zone 28. Support links 30 are tapered from peripherallinks 26 to central zone 28. Support links 30 may be tapered in width(as shown in FIG. 7), wall thickness, and/or other parameters capable ofinfluencing the structure's axial stiffness and flexibility along thelength of support link.

As previously stated, individual support links 30 may incorporatedifferent stiffness characteristics to tailor the stiffness profile ofthe support structure to the physiologic requirements. The proximal endsof the support links 30 are attached to the peripheral links 26 suchthat the intersection forms anchors 52 or defines an attachment point.Peripheral links 26 are configured significantly more flexible thansupport links 30 since peripheral links 26 maintain the integrity ofsupport structure 20 but do not transfer energy throughout tissueencompassed by the support structure.

FIG. 8 shows a heart that contains the support structure embodiment ofFIG. 7. Central zone 28 is located along the injured tissue region 24.The individual peripheral links 26 extend completely around the injuredtissue region 24 at distances defined by the individual support links30. These distances may be constant or may vary by changing the lengthand/or shape of each support link 30. The distances between peripherallinks 26 and central zone 28 also impact the stiffness profile of thesupport structure and influence the transfer of contraction andexpansion energy from viable tissue to the injured tissue zone 24.

The central zones of the various support structure embodiments discussedabove may be integral to support links 30 or alternatively may becomprised of one or more separate components that are attached to thesupport links. This separate component(s) may be fabricated from thesame material as the support links or a different material. Forinstance, compliant materials such as silicone, urethane, or otherbiological materials having high percent elongation characteristics maybe used.

FIGS. 9A and 9B show an alternative support structure embodiment thatcauses the width to expand as the length expands (or vice versa) andcauses the width to contract as the length contracts (or vice versa).For example, as an external force causes the length of the supportstructure to expand from position A1 to position A2, the width of thesupport structure expands from position B1 to position B2. The externalforce described in this embodiment may be, for example, movement ofviable tissue. The expansion or contraction energy is transferred fromthe actuated section of the support structure throughout the remainderof the support structure causing cardiac tissue, to which the supportstructure is attached, to expand or contract accordingly.

The characteristics of this support structure are substantiallydifferent than the flattened profile of any prior stent or stent-graft.Conventional stents or stent-grafts contract or minimally change inlength as the diameter is expanded. Stents or stent-grafts fabricatedwith the support structure geometry shown in FIGS. 9A and 9B expand inlength as the diameter is expanded. As such the support structureembodiment in FIGS. 9A and 9B may be fabricated as a complete tube andused as a stent or stent-graft (if the support structure is attached toat least one end of graft material).

The support structure embodiment shown in FIGS. 9A and 9B incorporatescells 40 interconnected by horizontal links 38 and vertical links 36that are attached to the cells at nodes 42. The cells also incorporatehinges 44 to permit expansion and contraction of the cells 40 inresponse to an external force. As the width (or length) of each cellexpands from W1 to W2 (or L1 to L2), cell nodes 42 located at verticallinks 36 and horizontal links 38 are deflected outward, about hinges 44,thereby causing the length (or width) of the cell to also expand from L1to L2 (or W1 to W2). This transfers the expansion force to adjacentcells, thereby propagating the expansion throughout the supportstructure. The converse is also true: as the width (or length) of eachcell contracts from W2 to W1 (or L2 to L1), the nodes are deflectedinward, causing the length (or width) of the cell to also contract fromL2 to L1 (or W2 to W1) and transferring the contraction force toadjacent cells.

The support structure embodiment of FIGS. 9A and 9B is shown as havingarrays of cells positioned equidistant along its the width and length,where each cell has a constant width and length in the relaxed position.Alternatively, the cells may be positioned such that vertical links 36and horizontal links 38 are generally not perpendicular. As such, thelength L1 (or width W1) of each cell may be decreased along the width B1(or length A1) of the support structure to produce a taper along thewidth (or length) of the support structure.

Other combinations of cell widths W1 and lengths L1 may be used totailor the stiffness and degree of ratio of expansion between the widthand length for the support structure to the geometry of the heart andthe amount of expansion and contraction desired throughout the supportstructure.

For example, to tailor this support structure embodiment so it may bepositioned apically, length A1 of the support structure may be taperedalong width B1 such that the length of each cell L1 decreases atspecified intervals and/or the length of each horizontal link 38decreases. Such modifications potentially impact the stiffness profileof the support structure; therefore, cell width T1, horizontal linkwidth T2, vertical link width T3, and/or wall thickness of each cell andlink may be decreased as the cells are tapered so as to compensate forthe increase in stiffness associated with decreasing the celldimensions.

Cell width T1, horizontal link width T2, vertical link width T3, and/orwall thickness of each cell and link may alternatively be varied topredefine the stiffness profile of the support structure, accommodatenonlinear expansion or contraction requirements throughout theventricles, or address anatomic variances that warrant changes insupport structure geometry or stiffness.

FIG. 10 shows a heart with the support structure embodiment of FIG. 9Battached to the left ventricle. Support structure 20 is centered aroundthe injured tissue region 24 to optimally transfer the expansion andcontraction forces from viable tissue to the injured tissue 24. Thesupport structure embodiment of FIG. 10 is shown in the enlargedconfiguration, reflecting the end-diastolic orientation and geometry ofthe support structure.

Positioning and securing support structure 20 to the surface of theheart chamber is preferably performed with the heart at end-diastole andwith the support structure in the enlarged orientation (either bypreshaping or manually stressing). In certain scenarios, the supportstructure may be configured to exert some contractile force throughoutthe cardiac cycle, even during end-diastole. To accomplish this, thesupport structure is positioned and secured to the tissue surface duringend-diastole with the support structure stressed into its expandedorientation. Securing the support structure to the heart duringend-diastole ensures better seating against the ventricle and theobserved spacing between attachment points 22 ensures optimal transferof contraction and expansion energy from the support link attachmentpoints to the injured tissue 24.

It should be noted that the steps of positioning and securing supportstructure 20 to the tissue surface may alternatively be performed atend-systole with support structure 20 in the contracted orientation, orat any phase in the cardiac cycle. It should also be noted that thepositioning and design of the support structure may bias the structuresuch that a continuous contractile force exerted by the elasticity ofthe support structure is applied even during end-diastole, a continuousexpansion force is applied even during end-systole, or a contractileforce is applied during relaxation and diastolic filling and anexpansion force is applied during contraction and systolic ejection.

The embodiments described above show the support structure attached tothe epicardial surface of the ventricles. Alternatively, as shown inFIG. 11, at least one support structure 86 and/or 88 may be secured tothe endocardial surface of at least one of the left ventricle 2 and theright ventricle 4. Any of the support structure embodiments describedabove may be modified to enable positioning the support structureagainst the endocardial surface. For purposes of discussion, theembodiment of FIG. 4 is shown as the left ventricular support structure86 and the right ventricular support structure 88 in FIG. 11. Thesupport structures 86 and 88 are configured such that the centralregions 28 of each is located at the apex 14 of the left ventricle 2 andright ventricle 4.

The LV support structure 86 is preferably preshaped to match theend-diastolic geometry and optimal size of the left ventricular cavity.Peripheral links 26 and support links 30 of LV support structure 86 donot interfere with the operation of mitral valve 48, the papillarymuscles, or the chordae tendonae. Support links 30 may be fabricatedwith spaces where the papillary muscles extend into the left ventricularcavity and where the chordae tendonae extend from the papillary musclesand connect to mitral valve 48. Support links 30 are distributedthroughout the endocardial surface of the left ventricle extending fromthe interventricular septum 46 completely around the left ventricularfree wall. As such, injured tissue regions extending into or locatedalong the interventricular septum may be covered by support structure86. Alternatively, the left ventricular support structure 86 may bedesigned to cover only the interventricular septum, the left ventricularfree wall, or other endocardial tissue region.

The RV support structure 88 is preferably preshaped to match theend-diastolic geometry and optimal size of the right ventricular cavity.Peripheral links 26 and support links 30 of RV support structure 88 donot interfere with the operation of the tricuspid valve 50, thepapillary muscles, or the chordae tendonae. Support links 30 may befabricated with spaces where the papillary muscles extend into the rightventricular cavity and where the chordae tendonae extend from thepapillary muscles and connect to the tricuspid valve 50. Support links30 are distributed throughout the endocardial surface of the rightventricle extending from the interventricular septum 46 completelyaround the right ventricular free wall. As such, injured tissue regionsextending into or located along the interventricular septum may becovered by the support structure 86. Alternatively, the rightventricular support structure 86 may be designed to cover only theinterventricular septum, the right ventricular free wall, or otherendocardial tissue region. For injured tissue isolated within theinterventricular septum, the right ventricle is the preferred locationto position and secure a support structure against the endocardialsurface in which the support structure is designed to solely causeexpansion and contraction of injured tissue along the interventricularseptum;

Support structures located along the endocardial surface of the rightand/or left ventricle may be combined with support structures locatedalong the epicardial surface to enhance the transfer of energy fromviable tissue to less viable or non-viable tissue, especially whenseveral injured tissue regions are dispersed throughout the heart. Thesupport structures may be independent such that the endocardial supportstructures are not attached to the epicardial support structures.Alternatively, individual support links of the endocardial supportstructures may be inserted through the myocardium and may be connectedto epicardial support structures so as to interconnect the expansion andcontraction of the endocardial support structures to the epicardialsupport structures. This is especially relevant when the injured tissueextends from the interventricular septum to the left ventricular freewall and the desired position of the support structure extends from theright ventricular endocardial surface of the interventricular septumthrough the myocardium of the right ventricle and along the epicardialsurface of the left ventricle. Other combinations of endocardially andepicardially positioned support structures may be used to address otherindications or injured tissue locations.

The various support structure embodiments described above exhibitisotropic, orthotropic, or anisotropic structural properties. It shouldbe noted that the embodiments of the invention may be modified toexhibit different structural properties (isotropic, orthotropic, oranisotropic) to match the inherent structural properties of the tissuesurface to which the support structure encompasses, or to tailor thesupport structure to specific tissue surface locations. They may also beconfigured to modify the structural properties of the tissue surface toreduce wall tension,. improve contractility, or otherwise change thefunctionality of the heart. It should also be noted that the structuralproperties of the support structures described above may be modified toaddress other applications as are known to those of skill in the art.

Support Structure Anchoring

The heart support structures described above typically are secured tothe epicardial surface and/or endocardial surface at attachment points22. A variety of bonding methodologies may be employed includingadhesives (fibrinogen, etc.), coagulating the surface to the supportstructure by heating the tissue, or mechanically anchoring the supportstructure to the tissue surface, a technique that is discussed below.The support structures may incorporate anchors that penetrate intotissue, holes to pass suture, flaps that become entangled in thetrabecula of the ventricles for endocardial support structures, or othermechanical securing mechanism with which to attach the heart supportstructure to the tissue surface. The heart support structure isalternatively secured to the tissue surface using commercially availableimplantable clips, staples, or other means.

FIG. 12A shows a support structure 20 that incorporates an anchor 52designed to penetrate into tissue. Anchor pins 54 extend radially awayfrom anchor 52 at acute angles to maintain the position of the anchorwithin the tissue surface, once positioned. Anchor pins 54 may extendfrom the anchor in curves as shown in FIG. 12B, along lines as shown inFIG. 12C, or in other orientations. As shown in FIG. 12D, supportstructure 20 is secure to the tissue surface after anchor 52 is insertedthrough the first heart surface (epicardium 60 or endocardium 58) andanchor pins 54 are constrained from axial movement by the myocardium 56.

Alternatively, the anchor may be inserted past the first heart surface(epicardium 60 or endocardium 58), through the myocardium 56, and pastthe second heart surface (endocardium 58 or epicardium 60) such that theanchor pins are constrained by the second heart surface. As shown inFIG. 12D, a tissue interface 18 spaces the support structure from thetissue surface, as will be described in detail below; even so, tissueinterface 18 must enable insertion of the anchor during positioning andsecuring of the support structure.

During deployment, anchor pins 54 may be constrained with a deliverytube or may be allowed to deflect into a reduced diameter as the anchoris inserted through the tissue surface (and tissue interface 18, ifany). The outward bias of anchor pins 54 causes them to extend radiallyonce positioned within the myocardium and prevent pulling the anchoraway from the tissue surface. The anchor shown in FIGS. 12A to d may befabricated from as a separate component that is bonded (e.g., spotwelding, soldering, adhesive bonding, or other suitable attachmentmeans) to the links of the support structure at predefined locations.Alternatively, the anchor may be cut (e.g., laser cutting, EDM, chemicaletching, water jet cutting, or other suitable process) from links in thesupport structure and thermally formed into the desired anchor andanchor pin shapes.

FIGS. 13A to 13C show an alternative anchor 52 embodiment. This anchor52 shapes anchor pin 54 into a screw configuration such that the anchoris inserted through the tissue surface 60 or 58 (and the tissueinterface 18, if any) as the anchor is rotated. This anchor 52 may be aseparate component that is independently rotatable relative to the linksof support structure 20, as shown in FIG. 13A. As such, a screw head 62may be formed in the proximal end of the anchor and used to rotate theanchor relative to the links of the support structure 20. Alternatively,the anchor pin may be integral to the links of support structure 20 andare straightened in a delivery tube for insertion through the tissuesurface 60 or 58 (and the tissue interface 18, if any). The deliverytube is removed from around the anchor pin, allowing the anchor pin toreturn towards its preformed shape once positioned in the myocardium 56.

The anchor pin of these embodiments may be configured with alternativegeometries to facilitate deployment and/or attachment of the supportstructure to the tissue surface. For example, a single anchor pin mayextend from the anchor as a hook which is capable of being insertedthrough the tissue surface by angling the anchor pin such that thedistal tip penetrates through the tissue surface and advancing the restof the anchor.

The anchors described previously may also be connected to anelectrosurgical generator capable of transmitting radio frequency (RF)energy to tissue contacting the anchors. As such, tissue adjacent theanchors resistively heats in response to exposure to the RF energy,causing the tissue to coagulate to the anchors and enhance the bondbetween the anchors (and thus the support structure) and the tissuesurface.

As shown in FIGS. 14A and 14B, holes 64 may be incorporated in the linksof support structure 20 such that commercially available suture 66(alternatively, clips or staples) may be inserted through one hole 64,past the tissue surface 60 or 58, partially through the myocardium 56,back through the tissue surface 60 or 58, and back through the secondhole 64. Once positioned, suture 66 is tied thereby securing the link ofthe support structure to the tissue surface. Alternatively, suture 66may be inserted through only one of the holes 64, or the suture 66 maybe passed around the width of a support structure link where no holesare required.

Tissue Interface

As shown in FIGS. 12D, 13B, and 14B, tissue interface 18 spaces supportstructure 20 from the surface of the heart (60 or 58), and inhibitsabrading the surface of the heart due to components of the supportstructure moving along the surface of the heart. Tissue interface 18 maybe a synthetic graft material, harvested biological material, or otherlubricious structure.

Alternatively, tissue interface 18 may be a spacer 90 incorporated insupport structure 20 at attachment point 22 to maintain separationbetween the epicardium 60 or endocardium 58 and the links of supportstructure 20, as shown in FIG. 13C. Spacers 90 are preferably thermallypreformed sections in the support structure located at the anchors 52,or desired attachment point 22, such that the links of the supportstructure are biased away from the tissue surface 60 or 58.

The support structure does not move relative to the tissue surface 60 or58 at the anchors and/or attachment points; therefore, the supportstructure may directly contact the tissue surface at those locations,realizing that the support structure will endothelialize orepithelialize at the locations where the support structure is inintimate tissue contact. For support structures that completely reflectmotion of the heart throughout the surface of the support structures,the entire support structure may be placed into intimate contact withthe tissue surface 60 or 58 and allowed to epithelialize orendothelialize and become integral with the heart.

The harvested biological material is preferably a section of thepericardium, which may be cut away, sized relative to the heart supportstructure, and positioned between the support structure and theepicardium. Other tissue such as submucosal tissue (e.g., that obtainedfrom the small intestine or other body organ) may be harvested, formedinto the desired geometry, and used as the heart interface. The use ofsubmucosal tissue is described in WO 98/19719 by Geddes, et al, entitled“Myocardial Graft Constructs”, the entirety of which is incorporatedherein by reference. Other biological materials such as collagen mayalternatively be formed into the desired geometry and used as the heartinterface.

The primary advantage of using biological tissue interface materialsover currently available synthetic materials is the reduction inadhesions, thrombosis for tissue interfaces that are exposed to bloodflow, or other tissue response that may adversely impact the function ofthe heart support structure. However, the heart support structureembodiments of the invention are equally effective at utilizing alltypes of tissue interface materials, biological and synthetic.

Synthetic tissue interface materials may be manufactured by extruding,injection molding, weaving, braiding, or dipping polymers such as PTFE,expanded PTFE, urethane, polyamide, polyimide, nylon, silicone,polyethylene, polyester, PET, composites of these representativematerials, or other suitable graft material. These materials may befabricated into a sheet, tubing, or other three-dimensional geometryusing one or a combination of the stated manufacturing processes. Tubingmaterials may be along at least one side to form a flattened profile.The synthetic bypass graft may be coated, deposited, or impregnated withmaterials, such as parylene, heparin solutions, hydrophilic solutions,thromboresistance substances (e.g., glycoprotein IIb/IIIa inhibitors),antiproliferative substances (e.g., Rapamycin), or other substancesdesigned to reduce adhesions, thrombosis (for heart interfaces exposedto blood flow), or mitigate other risks that potentially decrease thefunctionality of the heart support structure. In addition, syntheticbypass grafts may be seeded with endothelial cells or otherbiocompatible materials that further make the inner surface of thebypass graft biologically inert.

Deployment Systems

Surgical positioning and securing of the heart support structuresdescribed above to the epicardial tissue surface 60 involves arelatively large incision through the thoracic cavity to expose theheart. Surgical intervention enables accurate positioning and assuresoptimal securing of the support structure relative. During open heartsurgery, direct access to the epicardial surface of the heart enablessuturing or adhesively bonding the support structure to the heart; assuch, alternative anchoring mechanisms described above are notnecessarily requited. However, such anchoring mechanisms may providebenefit in reducing the time to attach the support structure to thesurface of the heart or improve the expanded (or contracted) orientationof the support structure relative to the end-diastolic (or end-systolic)orientation of the heart.

The support structure embodiments discussed in this invention aredirectly amenable to less invasive (i.e. minimally invasive) surgeryinvolving a thoracostomy or mini median sternotomy to access the heartand endoscopes to visualize the thoracic cavity.

The deployment system for such reduced access surgical applicationsleverages conventional port access techniques to produce an openingthrough the thoracic cavity. Trocars are commonly used to gain accessinto the thoracic cavity after puncturing through the intercostal space.Once the ports into the thoracic cavity are defined, the parietalpericardium is cut and the incision is extended to expose the epicardialsurface of the heart. As previously stated, the pericardium may be usedas the tissue interface between the support structure and the epicardialsurface of the heart.

The support structure is compressed into a reduced diameter by rollingfor relatively planar support structures, or folding, stretching, orotherwise bending for more three-dimensional support structures. Thecompressed support structure is positioned in a delivery sheath designedto feed the support structure past the port. Once inside the thoraciccavity, the support structure is expelled from the delivery sheath, atwhich point it expands towards its preformed resting shape.

At this point, the support structure is lined up relative to the desiredepicardial location and individual anchors are positioned through thetissue surface to secure the support structure to the tissue surface ateach attachment point. As previously stated, alternative securingmodalities may be used including adhesives, suture, thermal coagulation,implantable clips, staples, or other mechanism.

Conventional forceps, hemostats, and clamps are used to position theanchors. Alternatively, delivery tubes may compress the anchor pins intoa reduced diameter for insertion through the tissue surface. In such acase, the delivery tubes are beveled at their distal ends to penetratethrough the tissue surface and to provide a conduit to insert the anchorand position the anchor pin or pins into the myocardium.

When positioning the individual anchors at each attachment point, thesupport structure is continuously lined relative to the epicardialsurface and at end-diastole and the anchors are inserted through thetissue surface. This ensures the support structure is positioned in itsexpanded orientation against the ventricles in their expandedorientation producing a better match between the expansion andcontraction properties of the support structure to that of theventricles. When lining the anchors of the support structure, thesupport links may need to be stressed or preformed into their expandedorientation to ensure the support links are appropriately lined uprelative to the end-diastolic heart. As previously stated, the supportstructure may alternatively be attached to the heart during end-systole;at which case, the support structure is stressed or preformed into itscontracted orientation during the attachment process. Alternatively, theheart may be temporarily stopped while securing sections of the supportstructure to the epicardial surface.

When positioning the support structures against the endocardial surface,catheters are used to compress the support structure into a reduceddiameter. The catheters may be inserted percutaneously into the venousor arterial vasculature and routed to the desired heart chamber. Toaccess the left ventricle, a catheter is routed through the femoral orbrachial artery, around the aorta, past the aortic valve and into theleft ventricle. Alternatively, the catheter is passed through thefemoral or subclavian vein, into the right atrium, past the interatrialseptum (by use of a transseptal technique), into the left atrium, pastthe mitral valve annulus, and into the left ventricle. To access theright ventricle, the catheter is passed through the femoral orsubclavian vein, into the right atrium, past the tricuspid valve, andinto the right ventricle.

Once in the desired heart chamber, the catheter is positioned at theapex of the ventricle. The support structure is compressed within thecatheter by folding, stretching, or otherwise bending the supportstructure prior to inserting the catheter to the desired heart chamber.The support structure forms a three-dimensional geometry that closelymatches the endocardial surface (either at end-diastole or end-systole).The anchors of the support structure may contain flaps intended tobecome entangled in the trabecula of the ventricles or anchor pinscapable of becoming constrained in the myocardium once the anchor haspenetrated through the endocardial surface. A plunger, in the form of asecond steerable catheter, may be used to urge the anchors intoposition. Alternatively, the delivery catheter may be used as theplunger.

If any are used, the sheath and dilators of the deployment systems maybe constructed from polyethylene, polycarbonate, thermoplastic (such asPEEK, manufactured by Victrex PLC, United Kingdom), other polymer,metal, or metal alloy that may be extruded, injection molded, or swagedinto a tube having the desired cross-sectional profile. A taper andradius may be formed in the components of the deployment system bythermally forming the tubing into the desired shape or incorporatingsuch features in the injection molding cast. In addition, the componentsof the deployment system may incorporate a softer distal tip fabricatedby thermally bonding a short section of lower durometer tubing to thesheath or tapering the thickness of the sheath tubing.

To prevent the backflow of blood through deployment sheaths, hemostaticvalves may be used. The hemostatic valves prevent blood leakage butpermit insertion of the support structure through the sheath.

Electromagnetic Assist

It is within the scope of this invention to provide electromagneticassist devices that take advantage of the characteristics of the heartsupport structure of the invention to impart contraction throughout theheart or along a specific region of the ventricles. These devicesstrategically induce magnetic fields throughout the heart supportstructure to impart an expansion or contraction of the heart supportstructure, which then transfers energy to the heart chambers.

The electromagnetic assist device may function independent from thenatural contraction of the heart chambers to completely control thetiming of isovolumetric ventricular contraction, systolic ejection,isovolumetric relaxation, and diastolic filling. Alternatively, theelectromagnetic assist device may be synchronized to the inherentelectrical propagation of the heart, which passes from the SA Nodethrough the atria along the AV Node and through the ventricles. In doingso, the electromagnetic assist device times each phase of the cardiaccycle, as artificially created using the heart support structure,relative to the inherent electrical propagation of adjacent cardiactissue, thereby preserving the natural motion of the heart andresponding to biological stimuli for changing heart rate.

FIG. 15A shows a heart containing a support structure 20 thatincorporates electromagnetic coils 72 strategically positionedthroughout the links of the support structure. The embodiment of FIG.15A is the same as that of FIGS. 9A and 9B. Alternatively, previouslydescribed support structures may be used, provided they incorporatelinks to which the electromagnetic coils 72 may be attached and used toinduce a magnetic field designed to impart a contraction or expansion ofthe support structure.

U.S. Pat. No. 6,099,460 to Denker, incorporated herein by reference inits entirety, a heart that is artificially forced to contract inresponse to magnetic fields induced by electromagnets positioned on theexterior surface of the heart and/or interior of the heart. The '460patent does not incorporate a support structure to provide optimalcontraction and expansion, but relies solely on the attraction of theelectromagnets positioned on opposite sides of the heart chambers. Inaddition the injured or diseased tissue contracts differently thanviable tissue thus continuing to propagate the tissue remodeling of theinjured or diseased tissue. In addition, the '460 patent does not teachassisting in the diastolic filling of the heart, and therefore excludesone important phase in the cardiac cycle.

Electromagnetic cores 74 are positioned over horizontal links 38 ofsupport structure 20, as shown by an enlarged view of the supportstructure in FIG. 15B. Electromagnetic coils 72 are wound aroundelectromagnetic cores 74 and are routed to electromagnetic source 68either directly or via polarity switching unit 70 as shown in FIG. 15A.The leads of electromagnetic coils 72 that are directly connected to theelectromagnetic source are either connected to the positive terminal 76via positive lead 76 signal wires or the negative terminal 78 vianegative lead 78 signal wires. The leads of electromagnetic coils 72that are connected to the polarity switching unit 70 are eitherconnected to OUTA terminal 80 via lead (A) 80 signal wires or the OUTB82 terminal via lead (B) 82 signal wires. Polarity switching unit 70 isconnected to the positive and negative terminals of electromagneticsource 68. The polarity switching unit and the electromagnetic sourcemay also be grounded together. Polarity switching unit 70 changes theOUTA connection from the IN+ (that is routed to the positive terminal)to the IN− (that is routed to the negative terminal) and vice versa.

Simultaneously, polarity switching unit 70 changes the OUTB connectionfrom the IN− to the IN+ and vice versa. In switching the positive andnegative connections of an electromagnetic coil 72, the induced magneticfield along the electromagnetic coil alters its polarity accordingly. Assuch, the response of adjacent coils to the specific polarity protocolmay be specified to selectively produce an attraction between adjacentelectromagnets, thereby causing a contraction of the heart supportstructure, or to induce a repulsion between adjacent electromagnetsthereby causing an expansion of the heart support structure. The abilityto switch the polarity of at least one set of electromagnetic coils 72enables producing both an attraction and a repulsion thereby coveringthe complete cardiac cycle. The embodiment shown in FIG. 15A maintainthe polarity of a group of electromagnetic coils 72 constant and changesthe polarity of adjacent electromagnetic coils 72 to impart theattraction or repulsion force.

The period and amplitude of each pulse transmitted from theelectromagnetic source (directly or via the polarity switching unit) tothe electromagnetic coils determines the amount and duration of theattraction or repulsion force imparted to heart support structure 20 bythe electromagnetic assist device. Support structure 20 is essential tothe electromagnetic assist device in that it provides enhanced controlto and enables variability in the expansion and contraction throughoutthe surface of the heart. Changing the stiffness profile of the supportstructure 20 throughout the surface of the heart is more sensitive andeffective than varying the degree of attraction and repulsion betweenadjacent magnets.

FIG. 16A shows a heart incorporating another electromagnetic assistdevice embodiment. This embodiment has a different support structure 20embodiment attached only around the injured or diseased tissue. As such,the response of the electromagnetic assist device must be synchronizedwith the inherent electrical propagation throughout the heart. FIG. 16Bshows an enlarged view of the heart support structure in FIG. 16A.Support structure 20 incorporates horizontal links 38 and vertical links36 that interconnect electromagnetic cores 74 and associatedelectromagnetic coils 72. As described above, leads (76, 78, 80, or 82)of electromagnetic coils 72 are routed to terminals (positive ornegative) on electromagnetic source 68 or to terminals (OUTA or OUTB) onpolarity switching unit 70, which are routed to the terminals (positiveor negative) on the electromagnetic source 68.

As shown in FIG. 16A, a pacing controller 92 is connected to amplitudecontrol 96 of the electromagnetic source 68 and timing control 94 ofpolarity switching unit 70. Electrodes 98 and 100 are secured to theright atrium and left atrium respectively and atrial signals aretransmitted to pacing controller 92 which can acquire the atrialelectrograms. Ventricular signals from electromagnetic coils 72 may betransmitted through electromagnetic source 68 and/or polarity switchingunit 70 to pacing controller 92 which can filter the ventricularelectrograms. Pacing controller 92 utilizes the atrial and ventricularelectrograms to determine the activation of heart support structure 20by controlling the amplitude of the electromagnetic source and theswitching of the magnetic field polarity. In this way, the contractionand expansion of the heart support structure may be synchronized withthe natural movement of the heart.

Other Artificial Assists

The heart support structure embodiment shown in FIGS. 9A and 9B isdescribed as a potential support structure for the electromagneticassist device shown in FIG. 15A. This support structure embodiment mayalso be used in an assist device where an artificial external forceother than electromagnetic induction is used. The predetermined responsebetween the expansion (or contraction) of the width (or length) and thecorresponding expansion (or contraction) of the length (or width) makesthis support structure particularly amenable to an artificial externalforce that expands and/or contracts a first dimension and relies on thesupport structure to impart the expansion or contraction force to asecond dimension. Of course, the first dimension and/or the seconddimension described above may vary throughout the support structure. Alinearly actuated external force may be used to expand or contract adiscrete section of the support structure, relying on the supportstructure to transfer the expansion or contraction energy throughout theremaining support structure.

One such artificial external force involves attaching a length ofskeletal tissue to a section of the support structure and causing theskeletal tissue to contract and relax in response to pacing stimuli.This linear contraction and expansion is transferred throughout theentire support structure to impart the desired three-dimensionalcontraction and expansion responses.

Another artificial external force involves any type of motor capable ofexerting a linear force in response to an electrical current. The motorshould be capable of miniaturization to fit inside an implantable deviceand operate under battery power such that the battery life lasts foryears.

This invention has been described and specific examples of the inventionhave been portrayed. The use of those specific examples is not intendedto limit the invention in any way. Additionally, to the extent thatthere are variations of the invention which are within the spirit of thedisclosure and yet are equivalent to the inventions found in the claims,it is our intent that those claims cover those variations as well.

1-21. (canceled)
 22. A method of transferring energy from viable heart tissue to less viable or non-viable heart tissue by utilizing a natural motion of a heart, comprising: positioning a support structure over the viable and the less viable or non-viable heart tissue; and attaching the support structure to the viable heart tissue and to the less viable or non-viable heart tissue such that the support structure exerts a force against the less viable or non-viable heart tissue in response to the motion of the heart.
 23. The method of claim 22 wherein the support structure comprises at least one peripheral link and at least one support link.
 24. The method of claim 23 further comprising inducing a magnetic field such that the support structure contracts or expands.
 25. The method of claim 24 further comprising synchronizing the contraction or expansion with the natural motion of the heart. 26-31. (canceled)
 32. The method of claim 23 wherein the support structure is provided with a customized stiffness profile to maximize the restoration of systolic ejection and diastolic filling.
 33. The method of claim 32 wherein the customized stiffness profile includes predefining at least one of the width, wall thickness and length of the at least one support link.
 34. The method of claim 23 wherein the at least one peripheral link and the at least one support link define a geometry wherein expansion of a diameter of the support structure expands a length of the support structure.
 35. The method of claim 22 wherein the attaching the support structure is performed when the heart is at end-diastole.
 36. The method of claim 22 wherein the attaching the support structure is performed when the support structure is in an expanded configuration.
 37. The method of claim 22 further comprising delivering the support structure to a surface of the heart in a compressed configuration
 38. The method of claim 37 wherein the delivering the support structure to a surface of the heart comprises translating the support structure in the compressed configuration through a conduit.
 39. The method of claim 37 wherein the compressed configuration comprises at least one of folding, stretching, bending and rolling the support structure.
 40. The method of claim 22 wherein the heart tissue to which the support structure is attached is the epicardium.
 41. The method of claim 22 wherein the heart tissue to which the support structure is attached is the endocardium. 